Temporary reduction of blood pressure and sympathetic nerve activity in hypertensive patients after microvascular decompression.
OBJECTIVE
Experimental studies suggested neurovascular compression of the brain stem as a cause of hypertension. The aim of our prospective study was to investigate the effect of microvascular decompression in patients with severe hypertension with neurovascular compression on blood pressure and central sympathetic nerve activity in the long-term.


METHODS
Fourteen patients (4 males; mean age, 46+/-8 years) with essential hypertension underwent microvascular decompression of the brain stem. Vasoconstrictor muscle sympathetic nerve activity (recorded by microneurography: burst frequency, bursts/min) and blood pressure (24-hour profiles) were investigated before surgery and 7 days, 3 months, and every 6 months postoperatively.


RESULTS
Muscle sympathetic nerve activity was preoperatively elevated and decreased significantly postoperatively (35+/-13 bursts/min vs 20+/-9 bursts/min; P<0.01). Sympathetic activity remained reduced 3 months (19+/-8 bursts/min; P<0.01), 6 months (19+/-7 bursts/min; P<0.01), and 12 months (23+/-9 bursts/min; P<0.01) postoperatively. However, in the long-term, sympathetic nerve activity increased again (18 months after surgery: 28+/-10 bursts, not significant; 24 months postoperatively: 34+/-12 bursts/min, not significant). Systolic and diastolic blood pressure decreased from 162+/-6/98+/-5 mm Hg preoperatively to 133+/-6/85+/-4 mm Hg (7 days postoperatively; P<0.01); 136+/-5/86+/-4 mm Hg (3 months postoperatively; P<0.01); 132+/-4/85+/-4 mm Hg (6 months postoperatively; P<0.01); 132+/-3/85+/-5 mm Hg (12 months postoperatively; P<0.01); 132+/-5/84+/-5 mm Hg; P<0.01). Twenty-four months after microvascular decompression, blood pressure increased again up to 158+/-7/96+/-6 mm Hg, corresponding to the sympathetic nerve activity course.


CONCLUSIONS
Sympathetic nerve activity and blood pressure are temporary reduced by microvascular decompression in patients with severe hypertension with neurovascular compression. The data are a hint for sympathetic overactivity as a pathomechanism in this subgroup of patients.
Frank
Helga
H
Department of Nephrology, Klinikum rechts der Isar, Technische Universitaet Muenchen, Ismaninger Strasse 22, 81675 Munich, Germany. Helga.Frank@lrz.tum.de
Heusser
Karsten
K
Geiger
Helmut
H
Fahlbusch
Rudolf
R
Naraghi
Ramin
R
Schobel
Hans P
HP
D000328:Adult; D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery*; D017776:Autonomic Pathways / Q000503:physiopathology; D001488:Basilar Artery / Q000294:innervation / Q000503:physiopathology / Q000601:surgery; D001794:Blood Pressure / Q000502:physiology; D019299:Decompression, Surgical / Q000379:methods / Q000706:statistics & numerical data*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery*; D008297:Male; D008526:Medulla Oblongata / Q000098:blood supply / Q000503:physiopathology*; D008875:Middle Aged; D019635:Neurosurgical Procedures / Q000379:methods / Q000706:statistics & numerical data; D011446:Prospective Studies; D012008:Recurrence; D012154:Reticular Formation / Q000098:blood supply / Q000503:physiopathology; D017779:Sympathetic Fibers, Postganglionic / Q000503:physiopathology; D016896:Treatment Outcome; D014656:Vascular Surgical Procedures / Q000379:methods / Q000706:statistics & numerical data; D014661:Vasoconstriction / Q000502:physiology